The Verve Pipe, Willie Nile and More Set for LIGHT OF DAY WINTERFEST 2018

  by BWW News Desk -  Dec. 8, 2017 

Multi-platinum alterna-rockers The Verve Pipe, and exuberant rocker and Light of Day WinterFest fixture Willie Nile will lead the annual Asbury Angels Induction Show at LIGHT OF DAY WINTERFEST 2018, the 10-day festival (Jan. 5-15, 2018) entering its 18th year of raising money and awareness through the awesome power of music in order to defeat Parkinson's Disease and the Parkinsonisms, ALS and PSP, in our lifetime.

The Asbury Angels show - which honors and memorializes the lives and history of members of the Asbury Park musical community, "including but not limited to, musicians, tech support persons, DJs, journalists, club owners, record company personnel, managers and promoters" - will be held Friday, Jan. 12 at the Legendary Stone Pony, 913 Ocean Ave., in Asbury Park to kick off the final weekend of the charity festival's 18th edition. The Asbury Angels show, one of the most anticipated events at LOD WinterFest, is a six-hour marathon featuring more than a dozen acts celebrating the newest honorees, whose identities will be announced that evening. Doors open 6:30 p.m. Tickets $25 advance/$30 day of show at www.stoneponyonline.com, Ticketmaster, and at (732) 502-0600.

With a reputation for spectacular live performances, The Verve Pipe rose out of Michigan in the wake of Nirvana's success to dominate the mid-'90s airwaves with the inescapable, era-defining #1 smash single "The Freshmen." The band continues to be recognized worldwide for that and other radio hits "Photograph," "Hero," "Happiness Is," and "Never Let You Down." With a new lineup and a renewed energy and focus, lead singer/principal songwriter and founder Brian Vander Ark and the band continue to deliver original music distinguished by innovative arrangements, soul-searching lyrics and layered vocals. Willie Nile, who has played WinterFest every year since its inception, was hailed by the New York Times as "one of the most gifted singer-songwriters to emerge from the New York scene in years," and his Streets Of New York album was praised as "a platter for the ages" by UNCUT magazine. Rolling Stone listed The InnocentOnes as one of the "Top Ten Best Under-The-Radar Albums of 2011" and BBC Radio called it "THE rock 'n' roll album of the year." His single from that album, "One Guitar," was the "Top Pick of the Week" in USA Today, and has been adopted by Light of Day as its unofficial anthem.

The House of Independents, 572 Cookman Ave., in Asbury Park, will host a pair of major tribute shows to Prince and Led Zeppelin on consecutive evenings that weekend. Kashmir, the nation's #1 Led Zeppelin tribute show, takes over the House of Independents Friday, Jan. 12. The most authentic representation of Led Zeppelin on the modern national touring scene, Kashmir possesses the live stage show, sound and likeness to bring audiences and fans back to the days when the mighty Led Zeppelinruled the musical landscape. Doors 7 p.m. Tickets $20 advance; $25 day of show, Quincy Mumford and the Reason Why will lead the Tribute to Prince on Saturday, Jan. 13 at 7 p.m. Tickets $15 advance; $20 day of show. Mumford, an Asbury Park product, has a style described as "funk, soul and surf music, with a dash of reggae thrown in." Named by MSNBC as "1 of 10 up and coming young artists" in 2009, Mumford and his band have since performed over 800 shows around the U.S., including hosting "super jams" in certain cities, inviting local musicians to join them onstage for a jam session, covering songs from groups such as The Meters and James Brown. Tickets for Kashmir and the Tribute to Prince are available at www.houseofindependents.com.

Full lineups also have been announced for Sandy Mack's Wonder Jam, (Thursday, Jan. 11 at the Wonder Bar), Asbury Blues and the Full Tilt Boogie Bash (both being held Saturday, Jan. 13 at the Wonder Bar), and Songwriters by the Sea Boardwalk Crawl #2 (Jan. 14 at Langosta Lounge). Full details below.

Complete ticket and additional information for all LIGHT OF DAY WINTERFEST 2018 events at www.lightofday.org and on Facebook.

Light of Day WinterFest has gained international notoriety for surprise performances by Bruce Springsteen in 11 of the previous 17 years. In his best-selling autobiography, Born to Run, Springsteen revealed that his father suffered from Parkinson's Disease.

Last year's event raised $555,000 - a record amount - to combat Parkinson's disease, topping the previous year's record of $525,000, with the 17-year total approaching $4.5 million.

Beyond Asbury Park, LIGHT OF DAY WINTERFEST 2018 will include shows in New York City (Jan. 10 @ The Cutting Room), North Jersey (Jan. 5 in Montclair), and Philadelphia (Jan. 6, @ World Café Live). Those lineups will be announced at a later date. They are the culmination of a worldwide series of shows that began as a one-day event in Asbury Park and grew in the U.S. to a 10-day festival in the New Jersey/New York/Philadelphia metropolitan area.

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Here's the complete list of LIGHT OF DAY WINTERFEST 2018 shows to date:

Friday, JAN 5

LOD "NORTH JERSEY" Outpost in the Burbs, Montclair, NJ, 7pm, $TBA

Saturday, JAN 6

LOD "Philadelphia," The World Cafe, Upstairs, Philadelphia, Pa., 7pm, $TBA

Sunday, JAN 7

LOD "COVER ME: BEST OF THE JERSEY BAR BANDS", Stone Pony, All Ages, 1pm, $TBA

Monday, JAN 8

LOD "HAPPY MONDAYS", Wonder Bar, Mon., 21+, $TBA

Wednesday, JAN 10

LOD "NYC", The Cutting Room, 18+, 7pm, $75 VIP Reserved Seating, $45 GA Reserved Seating, $25 GA Standing

Thursday, JAN 11

LOD "FIRST NOTE", The Saint, Thurs.,18+, 6:30pm, $8adv/$12dos

LOD "SANDY MACK's WONDER JAM" - Karmic Juggernaut, Keith Kenny, Waiting on Mongo, Joe Miller, Mack Jamily Allstars, Strumberry Pie, Secret Sound, Acoustic Juggling Suns, Predator Dub Assassins, Stu Coogan (90.5 The Night) - Wonder Bar, Thurs.,21+, 7pm, $12

LOD "WINTERFEST 2018 KICK-OFF", House Of Independents, Thurs.,18+, 7pm, $20adv/$25dos

LOD "MONMOUTH UNIVERSITY'S BLUE HAWK RECORDS PRESENTS", Langosta Lounge, Thurs., All-Ages, 7pm, FREE ADMISSION

Friday, JAN 12

LOD "ASBURY ANGELS INDUCTION" - Boccigalupe & the Bad Boys, Miss Emily, Willie Nile, The Verve Pipe, Laura Crisci, Bobby Mahoney, Pat Toner, Bob Polding Band, Mad Kings, Peter Hogklint, Mike Rocket, more - Stone Pony, Fri., All Ages, 6:30pm, $25adv/$30dos

LOD KASHMIR - The Live Led Zeppelin Show with Colossal Street Jam, Bitter Crush - House Of Independents, Fri.,18+, 7pm, $20 adv/$25 dos

LOD "ROCK HEAVY", The Saint, Fri.,18+, 8pm, $8adv/$12dos

LOD "OPEN MIC", Wonder Bar, Fri., 21+, 6pm, $12

LOD TBA, McLoone's Supper Club, Fri., All Ages, Doors/Dinner 6pm/ Show 8pm, $TBA

LOD "LATE NIGHT FRIDAY" Langosta Lounge, l, Friday, 21+, 9pm, FREE ADMISSION

LOD "TBA" Paramount Theater, Fri., All Ages, 8pm, $TBA

Saturday, JAN 13

LOD "BOB'S BIRTHDAY BASH", Paramount Theater, Sat, All Ages, 6pm, $43-$205

LOD "ROCK", The Saint, Sat., 18+, 7:30pm, $8adv/ $12dos

LOD TBA, McLoone's Supper Club, Sat., All Ages, Noon, $TBA

LOD TBA, McLoone's Supper Club, Sat., 18+, 7pm, $TBA

LOD "LATE NIGHT SATURDAY", Langosta Lounge, Sat., Jan. 17, 21+, 10pm, FREE ADMISSION

LOD TRIBUTE TO PRINCE, STARRING QUINCY MUMFORD & THE REASON WHY, House Of Independents, Sat., 18+, 8pm, $15 adv/$20 dos

LOD "ASBURY BLUES" - Billy Walton Band, Karen Phillips, Tony Tedesco & Full Fathom 5, James Dalton, Chuck Lambert, Pam McCoy, Normin Seldin, Joe Whyte, RB3, String Bean, Papa John Bug & The Jam Band - Wonder Bar, Sat., All Ages, Noon, $12/$15

LOD "FULL TILT BOOGIE BASH" - Billy Hector, Laura Crisci, Christine Martucci, Colton Kaiser, Mike Miz, Slyders, Sharon Lasher, Dawg Whistle, Strumberry Pie - Wonder Bar, Sat., 21+, 7pm, $12/$15

LOD "DOWNTOWN - ASBURY UNDERGROUND," curated by Pat Schiavino and Asbury Underground. Noon - 7PM Over 20 venues! FREE ADMISSION

Sunday, JAN 14

LOD "SONGWRITERS BY THE SEA BOARDWALK CRAWL", Watermark, Sun., All Ages, Noon, $15

LOD "SONGWRITERS BY THE SEA BOARDWALK CRAWL" - Bruce Tunkel, Karen Mansfield, Pat Guadagno, Sams Sims/Kyle Ward, Frank Lombardi, Joshua, Scott Elk - Langosta Lounge, Sun., All Ages, 3pm, $15

LOD "SONGWRITERS BY THE SEA BOARDWALK CRAWL", McLoone's Supper Club, Sun., All Ages, 6pm, $20

LOD "KID'S ROCK", Stone Pony, Sun., All Ages, Noon, $15

LOD "MUSICIANS ON A MISSION", The Saint, Sun., 18+, Noon, $10

LOD "LAST NOTE", The Saint, Sun., 18+, 7:30pm, $8adv/$12dos

Monday, JAN 15

LOD "GOODBYE BRUNCH," Toast, Mon., All Ages, 10:30a-1:30p.

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The Light of Day Foundation, Inc., utilizes the awesome power of music to raise money and awareness in its continuing battle to defeat Parkinson's disease and related neuro-degenerative diseases, specifically Progressive Supranuclear Palsy (PSP) and Amyotrophic Lateral Sclerosis (ALS), within our lifetime. The Foundation's mission is to fund research into possible cures, improved treatments and support for patients who suffer from those diseases, their families and their caregivers to help improve their quality of life. Gifts to the Light of Day Foundation, Inc. are tax-deductible to the full extent of the Internal Revenue Code. The Light of Day Foundation, Inc. is designated by the IRS as a not-for-profit 501(c) (3) organization. The Light of Day Foundation, Inc.'s Federal ID # is 20-1560386. Light of Day - the concerts and the organization - grew from a birthday party and fund-raiser held in 1998 at the Downtown Cafe in Red Bank to celebrate the 40th birthday of artist manager and music industry veteran Bob Benjamin, who was diagnosed with Parkinson's disease in 1996.

https://www.broadwayworld.com/new-jersey/article/The-Verve-Pipe-Willie-Nile-and-More-Set-for-LIGHT-OF-DAY-WINTERFEST-2018-20171208#

Senior center class combats Parkinson’s through song

By Kyle Jensen Saturday, December 9, 2017

Kyle Jensen / The Record — Scott Martin (left) and class organizer Mel Watson (center) pretend to play the harmonica while John Raabe (right) sings.

When members of Island Senior Resources’ Parkinson’s Support Group first learned about the health benefits music can have on those living with the disease, they wanted to inject tunes into their routine.

But when a vocal coach was hired and attempted to focus on the quality of their singing, things simply didn’t pan out. The singers didn’t care if they were out of key. They just wanted to exercise their pipes.

Group member Ed Wootten started thinking about informal ways to sing together. Then it hit him — what about karaoke?

“WE WANTED something that just let us do the singing,” Wootten said. “I always thought karaoke was something for the bar after a few drinks. It turns out this is all we needed here.”

The Parkinson’s sing-a-long sessions are held from 2:30-3:30 p.m. every Tuesday at the senior center in Bayview. Organized by Mel Watson, who runs the senior center’s Parkinson’s Support Group and the Time Together adult day program, the classes are intentionally informal.

Watson and the attendees grab a chair in front of the TV and select the song of their choosing, with accompanying words to sing along to.

As the song begins, participants sing in unison, focusing on volume more than anything else. That’s what really matters for people living with the neurodegenerative disease.

CLASSES COST $10 per person. Participants can bring caregivers and families for no additional cost.

Working the vocal chords combats some of the neuron degeneration that comes with the disease. It’s a common side effect for people with Parkinson’s to have a shrinking voice, which can become softer over time as neurons slowly die off. It can lead to some Parkinson’s patients being difficult to understand.

This was all too familiar for group member Scott Martin until he became the sing-a-long group’s de facto bass and baritone.

“I have a naturally deep voice, so it relaxes really easily when I talk,” Martin said. “I didn’t give it the volume people need to hear. After singing every now and then, I automatically give it more volume.”

“Being able to keep up your voice so other people can understand what you’re saying makes an impact in all facets of your life.”

AS IS the case with music in general, singing has numerous other health benefits on the brain. Constantly engaging in activities is a good way to combat the die-off of neurons, Watson said, and can also bring a rhythm into their lives that can facilitate better body movement.

It also keeps the brain active, which can fight the loss of neurons.

It’s a situation where if you don’t use it, you can lose it, Watson says.

“There’s a lot of research on both Parkinson’s and dementia that shows health is improved with singing and music,” group member John Raabe said. “It helps people hang onto their neurons better.”

There’s also a social aspect to the classes that group members say is invaluable. They’ve become good friends who “are all in this together,” according to Martin.

PARKINSON’S CAN often lead to social isolation, Watson said, as people living with the disease can become distraught with their inability to do things they used to do. With these sing-a-long sessions, group members get out of the house in a platform where they can relate to others going through a similar situation.

Watson says their situations can be difficult for people without the disease to understand. The karaoke sessions can provide that outlet.

“It’s a group that’s really active in trying to prolong their quality of life,” Watson said. “There’s a well-known path for people with Parkinson’s, and it’s not a pretty one.

“But I really believe in the power of music, and I can see that play out here every week.”

http://www.southwhidbeyrecord.com/news/senior-center-class-combats-parkinsons-through-song/

Genetics Study Adds Further Evidence That Education Reduces Alzheimer’s Risk

NEUROSCIENCE NEWS  DECEMBER 9, 2017
Source: University of Cambridge.

A new study adds further weight to the theory that being educated may help to stave off Alzheimer’s disease.

Exactly how education might reduce the risk of Alzheimer’s is uncertain. Previous studies have shown that the same amount of damage in the brain is associated with less severe and less frequent Alzheimer’s in people who have received more education. One possible explanation is the idea of ‘cognitive reserve’ – the ability to recruit alternative brain networks or to use brain structures or networks not normally used to compensate for brain ageing. Evidence suggests that education helps improve brain wiring and networks and hence could increase this reserve. NeuroscienceNews.com image is in the public domain.

The theory that education protects against Alzheimer’s disease has been given further weight by new research from the University of Cambridge, funded by the European Union. The study is published today in The BMJ.

Alzheimer’s disease is the leading cause of dementia. Its chief hallmark is the build of ‘plaques’ and ‘tangles’ of misshapen proteins, which lead to the gradual death of brain cells. People affected by Alzheimer’s experience memory and communication problems, disorientation, changes in behaviour and progressive loss of independence.

The causes of Alzheimer’s are largely unknown, and attempts to develop drug treatments to halt or reverse its effects have been disappointing. This has led to increasing interest in whether it is possible to reduce the number of cases of Alzheimer’s disease by tackling common risk factors that can be modified. In fact, research from the Cambridge Institute of Public Health has shown that the incidence of Alzheimer’s is falling in the UK, probably due to improvements in education, and smoking reduction and better diet and exercise.

“Many studies have shown that certain risk factors are more common in people with Alzheimer’s disease, but determining whether these factors actually cause Alzheimer’s is more difficult,” says Professor Hugh Markus from the Department of Clinical Neurosciences at the University of Cambridge.

“For example, many studies have shown that the more years spent in full time education, the lower the risk of Alzheimer’s. But it is difficult to unravel whether this is an effect of education improving brain function, or whether it’s the case that people who are more educated tend to come from more wealthy backgrounds and therefore have a reduction in other risk factors that cause Alzheimer’s disease.”

Professor Markus led a study to unpick these factors using a technique known as ‘Mendelian randomisation’. This involves looking at an individual’s DNA and comparing genes associated with environmental risk factors – for example, genes linked to educational attainment or to smoking – and seeing which of these genes are also associated with Alzheimer’s disease. If a gene is associated with both, then it provides strong evidence that this risk factor really does cause the disease.

As part of a project known as CoSTREAM, researchers studied genetic variants that increase the risk of a variety of different environmental risk factors to see if these were more common in 17,000 patients with Alzheimer’s disease. They found the strongest association with genetic variants that predict higher educational attainment.

“This provides further strong evidence that education is associated with a reduced risk of Alzheimer’s disease,” says first author Dr Susanna Larsson, now based at the Karolinska Institute, Sweden. “It suggests that improving education could have a significant effect on reducing the number of people who suffer from this devastating disease.”

Exactly how education might reduce the risk of Alzheimer’s is uncertain. Previous studies have shown that the same amount of damage in the brain is associated with less severe and less frequent Alzheimer’s in people who have received more education. One possible explanation is the idea of ‘cognitive reserve’ – the ability to recruit alternative brain networks or to use brain structures or networks not normally used to compensate for brain ageing. Evidence suggests that education helps improve brain wiring and networks and hence could increase this reserve.

The researchers also looked at other environmental risk factors, including smoking, vitamin D, and alcohol and coffee consumption. However, their results proved inconclusive. This may be because genes that predispose to smoking, for example, have only a very small effect on behaviour, they say.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Funding: The study was supported by the European Union’s Horizon 2020 Research and Innovation Programme.

Source: Craig Brierley – University of Cambridge

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is in the public domain.

Original Research: Full open access research for “Modifiable pathways in Alzheimer’s disease: Mendelian randomisation analysis” by Susanna C Larsson, Matthew Traylor, Rainer Malik, Martin Dichgans, Stephen Burgess, and Hugh S Markus in The BMJ. Published online December 7 2017 doi:10.1136/bmj.j5375

Abstract

Modifiable pathways in Alzheimer’s disease: Mendelian randomisation analysis

Objective To determine which potentially modifiable risk factors, including socioeconomic, lifestyle/dietary, cardiometabolic, and inflammatory factors, are associated with Alzheimer’s disease.

Design Mendelian randomisation study using genetic variants associated with the modifiable risk factors as instrumental variables.

Setting International Genomics of Alzheimer’s Project.

Participants 17 008 cases of Alzheimer’s disease and 37 154 controls.

Main outcome measures Odds ratio of Alzheimer’s per genetically predicted increase in each modifiable risk factor estimated with Mendelian randomisation analysis.

Results This study included analyses of 24 potentially modifiable risk factors. A Bonferroni corrected threshold of P=0.002 was considered to be significant, and P<0.05 was considered suggestive of evidence for a potential association. Genetically predicted educational attainment was significantly associated with Alzheimer’s. The odds ratios were 0.89 (95% confidence interval 0.84 to 0.93; P=2.4×10−6) per year of education completed and 0.74 (0.63 to 0.86; P=8.0×10−5) per unit increase in log odds of having completed college/university. The correlated trait intelligence had a suggestive association with Alzheimer’s (per genetically predicted 1 SD higher intelligence: 0.73, 0.57 to 0.93; P=0.01). There was suggestive evidence for potential associations between genetically predicted higher quantity of smoking (per 10 cigarettes a day: 0.69, 0.49 to 0.99; P=0.04) and 25-hydroxyvitamin D concentrations (per 20% higher levels: 0.92, 0.85 to 0.98; P=0.01) and lower odds of Alzheimer’s and between higher coffee consumption (per one cup a day: 1.26, 1.05 to 1.51; P=0.01) and higher odds of Alzheimer’s. Genetically predicted alcohol consumption, serum folate, serum vitamin B12, homocysteine, cardiometabolic factors, and C reactive protein were not associated with Alzheimer’s disease.

Conclusion These results provide support that higher educational attainment is associated with a reduced risk of Alzheimer’s disease.

“Modifiable pathways in Alzheimer’s disease: Mendelian randomisation analysis” by Susanna C Larsson, Matthew Traylor, Rainer Malik, Martin Dichgans, Stephen Burgess, and Hugh S Markus in The BMJ. Published online December 7 2017 doi:10.1136/bmj.j5375

http://neurosciencenews.com/education-alzheimers-8147/

3D MINI BRAINS ACCELERATE RESEARCH FOR REPAIRING BRAIN FUNCTION

December 8, 2017

Source: Houston Methodist.

Researchers have developed a new method of reducing the time it takes to grow mini brain models in the lab. This may accelerate research into diseases and injury that affect the nervous system.

Three-dimensional neural circuit “asteroid” composed of neurons (blue) and astrocytes (red and green) generated from human pluripotent stem cells. NeuroscienceNews.com image is credited to Robert Krencik and Jessy van Asperen.

The Houston Methodist Research Institute is making mini brains from human stem cells that put researchers on a fast track to repair the nervous system after injury or disease of the brain and spinal cord.

Houston Methodist neuroscientist Robert Krencik, Ph.D., and his team have developed a new system to reduce the time it takes to grow these brain models, which will give them the ability to screen drugs and study what’s behind disease-causing mutations more quickly. Their findings are described in an article titled “Systematic three-dimensional coculture rapidly recapitulates interactions between human neurons and astrocytes,” in the Dec. 12 issue of Stem Cell Reports.

“We always felt like what we were doing in the lab was not precisely modeling how the cells act within the human brain,” Krencik said. “So, for the first time, when we put these cells together systematically, they dramatically changed their morphological complexity, size and shape. They look like cells as you would see them within the human brain, so now we can study cells in the lab in a more natural environment.”

And why is this important? Krencik says cells grown in traditional lab cultures are put on a flat petri dish, broken up and otherwise manipulated, disturbing their interactions. This results in not being able to reproduce the form, structure and developmental growth of the brain’s cells in the lab, leading to very simplistic-looking and immature cells. In the human brain, however, these cells are very complex-looking and interact in intricate ways with each other and the environment. New technologies are now focused on 3-D culture systems, but the exhaustive time for these studies is not feasible for accelerating discoveries.

“Normally, growing these 3-D mini brains takes months and years to develop,” Krencik said. “We have new techniques to pre-mature the cells separately and then combine them, and we found that within a few weeks they’re able to form mature interactions with each other. So, the length of time to get to that endpoint for studies is dramatically reduced with our system.”

Krencik’s lab focused on a star-shaped cell type called astrocytes, because they are a key factor in getting the brain’s neurons to connect and talk to each other by helping to increase the number and strength of neuronal connections in the brain and spinal cord. They are involved in most neural diseases and also are responsible for maintaining a healthy nervous system. With the model Krencik’s team bioengineered, the incorporation of astrocytes accelerated the connections of the surrounding neurons.

Krencik’s group is the first to specifically engineer astrocytes into these 3-D mini brains. By doing so, this led to the accelerated maturation of both the astrocytes and the surrounding neurons. Introducing them for the first time in this paper, he coined these bioengineered mini brains “asteroids” to distinguish them from other types of 3-D sphere cultures, known as organoids. Krencik’s “asteroids” contain specific populations of astrocytes, whereas organoids have undefined numbers and types of cells.

“Using our system, we can generate mature astrocytes and have them interact intimately with neurons to a greater extent than has been done before,” Krencik said. “Unlike other cells in the brain and in the rest of the body, astrocytes have unique properties in humans. It’s thought they are partly responsible for the unique cognitive functions of humans and also may underlie aspects of human diseases, such as Alzheimer’s and autism spectrum disorders.”

Ultimately, Krencik is using these “asteroids” to form functional neural circuits that researchers can experimentally manipulate for developing treatments and deciphering what makes diseases tick. Krencik says they can make induced pluripotent stem cells, commonly termed iPS cells, from any disease or patient and then form these mini brains to study the disease process, as well as screen therapeutic compounds on them to aid in the development of drugs. Within about five years, his goal is to use this system to develop clinical trials to improve or regenerate a person’s impaired nervous system.

ABOUT THIS NEUROSCIENCE RESEARCH ARTICLE

Researchers collaborating with Krencik on this paper include Philip J. Horner, Nupur Basu, Caroline Cvetkovic and Saba Barlas with Houston Methodist Research Institute; Michael E. Ward with the NIH’s National Institute of Neurological Disorders and Stroke; and Li Gan, David H. Rowitch, Erik M. Ullian, Robert Chen, Connor Ludwig, Chao Wang, Kyounghee Seo and Jessy V. van Asperen with the University of California, San Francisco.

Funding: The work was supported by a Paul G. Allen Family Foundation Award, SFARI Award (345471), an NIH National Institute of Mental Health grant (R01MH099595-01), a gift from the That Man May See foundation, an NIH National Eye Institute Core Grant for Vision Research (EY002162), and a Research to Prevent Blindness Unrestricted Grant.

Source: Lisa Merkl – Houston Methodist

Publisher: Organized by NeuroscienceNews.com.

Image Source: NeuroscienceNews.com image is credited to Robert Krencik and Jessy van Asperen.

Original Research: Full open access research for “Systematic Three-Dimensional Coculture Rapidly Recapitulates Interactions between Human Neurons and Astrocytes” by Robert Krencik, Kyounghee Seo, Jessy V. van Asperen, Nupur Basu, Caroline Cvetkovic, Saba Barlas, Robert Chen, Connor Ludwig, Chao Wang, Michael E. Ward, Li Gan, Philip J. Horner, David H. Rowitch, and Erik M. Ullian in Stem Cell Reports. Published online November 30 2017 doi:10.1016/j.stemcr.2017.10.026

Abstract

Systematic Three-Dimensional Coculture Rapidly Recapitulates Interactions between Human Neurons and Astrocytes

Highlights

•Novel three-dimensional “asteroid” coculture system is described

•Complex human astrocyte-specific morphology is generated in vitro

•This system produces rapid and tight association of astrocytes with synapses

Summary

Human astrocytes network with neurons in dynamic ways that are still poorly defined. Our ability to model this relationship is hampered by the lack of relevant and convenient tools to recapitulate this complex interaction. To address this barrier, we have devised efficient coculture systems utilizing 3D organoid-like spheres, termed asteroids, containing pre-differentiated human pluripotent stem cell (hPSC)-derived astrocytes (hAstros) combined with neurons generated from hPSC-derived neural stem cells (hNeurons) or directly induced via Neurogenin 2 overexpression (iNeurons). Our systematic methods rapidly produce structurally complex hAstros and synapses in high-density coculture with iNeurons in precise numbers, allowing for improved studies of neural circuit function, disease modeling, and drug screening. We conclude that these bioengineered neural circuit model systems are reliable and scalable tools to accurately study aspects of human astrocyte-neuron functional properties while being easily accessible for cell-type-specific manipulations and observations.

“Systematic Three-Dimensional Coculture Rapidly Recapitulates Interactions between Human Neurons and Astrocytes” by Robert Krencik, Kyounghee Seo, Jessy V. van Asperen, Nupur Basu, Caroline Cvetkovic, Saba Barlas, Robert Chen, Connor Ludwig, Chao Wang, Michael E. Ward, Li Gan, Philip J. Horner, David H. Rowitch, and Erik M. Ullian in Stem Cell Reports. Published online November 30 2017 doi:10.1016/j.stemcr.2017.10.026

http://neurosciencenews.com/mini-brain-function-8135/

Low-frequency Brain Stimulation Improves Parkinson’s Patients’ Thinking Ability, Study Shows

 DECEMBER 7, 2017   BY ALICE MELÃO 

Using low-frequency electrical pulses to stimulate a deep brain region can improve the cognitive function of people with Parkinson’s and other neurological diseases, a study suggests.

The U.S. Food and Drug Administration has already approved high-frequency deep brain stimulation as a way to treat Parkinson’s. A team at the University of Iowa’s Neuroscience Institute showed that low-frequency stimulation is also a promising approach.

Their study also showed for the first time that there is a direct link between the thinking region of the brain — the frontal cortex — and the area that controls movement — the subthalamic nucleus, or STN.

The research, “A human prefrontal-subthalamic circuit for cognitive control,” was published in the journal Brain.

“It’s not very often that you identify a new connection in the human brain,” Dr. Nandakumar Narayanan, an assistant professor of neurology at the university’s Carver College of Medicine, said in a news release.

“The existence of this hyperdirect pathway from the prefrontal cortex to the STN has been bandied about for around a decade, but this is the first time we’ve experimentally shown that it exists and functions in people,” added Narayanan, the study’s senior author.

Jeremy Greenlee, a medical school neurosurgeon who co-authored the study, performed more than 30 surgeries to implant deep brain stimulation electrodes in Parkinson’s patients.

During the surgeries, while patients were still awake, the team recorded the activity in their  subthalamic nucleus and other brain regions.

Researchers also asked patients to do a simple cognitive task while they were in surgery. As they did so, the team stimulated their frontal cortex, recording activity in brain areas connected to it. This allowed the team to identify signals that suggested a direct connection between brain regions.

“We were able to evoke a response to show the functional connection,” Greenlee said. “The very fast response suggests a single, direct synaptic connection — that is what hyperdirect means.”

In follow-up visits, patients were asked to perform interval timing tasks again. Researchers alternated between setting their brain electrodes to high frequency or low frequency, or not sending electrical pulses at all.  Surprisingly, patients performed their task faster with low-frequency stimulation than with high-frequency or no stimulation.

“If we stimulate the STN and change cortical activity, we can actually change behavior in a beneficial way, improving the patients’ cognitive performance,” Narayanan said.

“It is exciting to potentially have a way to improve cognition that could be life-changing for patients,” Greenlee said.

This study was funded in part by two U.S. government agencies — the National Institute of Neurological Disorders and Stroke and the National Institute on Deafness and Other Communication Disorders.

https://parkinsonsnewstoday.com/2017/12/07/study-shows-that-low-frequency-pulses-improve-parkinsons-patients-thinking-ability/

A New CRISPR Technique Reverses Diseases in Mice

by Brad Jones on December 7, 2017

CRISPR, No Cuts

CRISPR-Cas9 technology allows scientists to insert or remove genes by making a cut in a DNA molecule; an ability that has applications ranging from the creation of pigs with lower levels of body fat to the eradication of certain diseases. However, the technique also has the potential to create genetic mutations that may produce undesired side effects.

https://youtu.be/MnYppmstxIs

With that in mind, a team of researchers set out to develop a take on CRISPR-Cas9 technology that wouldn’t require the DNA to be cut at all. A trial of their technique was successfully used on mice to treat several diseases. The study proves, for the first time, that the phenotype of an animal can be altered via epigenetic editing while ensuring the integrity of the DNA is preserved and no mutations are introduced.

“Cutting DNA opens the door to introducing new mutations,” said senior author Juan Carlos Izpisua Belmonte in a press release. “That is something that is going to stay with us with CRISPR or any other tool we develop that cuts DNA. It is a major bottleneck in the field of genetics – the possibility that the cell after the DNA is cut may introduce harmful mistakes.”

Manipulation Machinery

The technique uses two adeno-associated viruses (AAV) to introduce genetic manipulation machinery to cells in post-natal mice. One contains the gene for the Cas9 enzyme, and the other contains a transcriptional activator and is outfitted with a short single guide RNA (sgRNA) which determines the exact position the enzyme needs to bind to within the mouse genome. Since the sgRNA is only comprised of fourteen or fifteen nucleotides, compared to the twenty that are used in most CRISPR-Cas9 procedures, no cut is required.

When this complex is placed near the DNA set to be modified, it promotes the expression of a particular gene. The same basic principle could be implemented to activate almost any gene or genetic pathway without the potential for unwanted mutations.

In tests using a mouse model of acute kidney disease, the technique was seen to activate damaged or silenced genes, allowing the kidney to function normally. It proved useful for helping liver cells regain the ability to produce insulin, which contributed to a mouse’s recovery from type 1 diabetes.

The team also demonstrated the capacity to recover muscle growth and function in mouse models of muscular dystrophy, a condition that’s linked to a gene mutation. But instead of seeking to correct it, the expression of genes in the same pathway was actually increased — which then took precedence over the mutation.

“We are not fixing the gene; the mutation is still there,” said Belmonte, “Instead, we are working on the epigenome and the mice recover the expression of other genes in the same pathway. That is enough to recover the muscle function of these mutant mice.”

From Mice to Humans

Based on these early trials the method doesn’t seem to produce any precarious side effects, but before any clinical testing gets underway, the researchers will carry out further studies to assess safety, practicality, and efficiency.

Researchers hope the technique could lend itself to developing treatments for a wide variety of neurological disorders, including Alzheimer’s and Parkinson’s disease, by spawning healthy neurons in the same way that it addressed kidney disease in mice. That said, there’s still a long way to go before the technique could be tested in humans.

“There are still multiple steps that need to be examined before applying this method in human patients,” co-first author Hsin-Kai Liao told Futurism. “For example, it must be determined whether host immune responses against the AAV-CRISPR/Cas9 Target Gene Activation system arise in mice or large animals. Safety and ethical considerations will also have to be addressed before bringing this technique to human patients.”

The potential for a safe, efficient method of addressing ailments ranging from Parkinson’s disease to muscular dystrophy is certainly very compelling, but early successes while testing on mice don’t necessarily mean that the technique will be viable for humans. Once the questions pertaining to host immune responses and ethical considerations have been addressed, the team hopes to have a clearer timeline regarding clinical trials.

References: Eurekalert, Cell

https://futurism.com/new-crispr-technique-reverses-diseases-in-mice/